BACKGROUND: The involvement of nitric oxide (NO) in vagal control and vasoactive intestinal polypeptide (VIP)-induced effects on antral motility was studied using isolated perfused preparations of porcine gastric antrum with intact vagal innervation. METHODS: The presence of NO and VIP-producing neurons was studied using immunohistochemistry and histochemical techniques. Widespread, but not total, co-localization of NO and VIP immunoreactivity was found in the submucosa and in the muscle layers. RESULTS: Electrical stimulation of the vagus nerves for 5 min (8 Hz, 10 mA, 4 msec) increased the motility index from 2.47 = 0.44 to 11.50 +/- 2.02 (n = 5). This effect was not influenced by the two NO synthase inhibitors N-nitro-L-arginine methyl ester (10(-4) M) and NG-nitro-L-arginine (10(-5) M). However, infusion of inhibitors increased the spontaneous motility index from 2.40 +/- 0.08 to 5.36 +/- 1.08 (P < 0.05) and 3.05 +/- 1.10 to 4.14 +/- 1.04 (P < 0.05), respectively. The addition of L-arginine reversed this effect. Infusion of VIP 2 x 10(-9)M decreased the motility index from 2.32 +/- 0.43 to 1.32 +/- 0.27 (P < 0.05), an effect that was preserved during NO synthase inhibition. Electrical vagus stimulation increased the release of VIP to the venous effluent, an effect that persisted during NO synthase inhibitors. CONCLUSION: We conclude that NO-producing nerves seem to have a tonic inhibitory action on the porcine antral motility, but are not involved in the motor effects of vagal stimulation or VIP infusion.
BACKGROUND: The involvement of nitric oxide (NO) in vagal control and vasoactive intestinal polypeptide (VIP)-induced effects on antral motility was studied using isolated perfused preparations of porcine gastric antrum with intact vagal innervation. METHODS: The presence of NO and VIP-producing neurons was studied using immunohistochemistry and histochemical techniques. Widespread, but not total, co-localization of NO and VIP immunoreactivity was found in the submucosa and in the muscle layers. RESULTS: Electrical stimulation of the vagus nerves for 5 min (8 Hz, 10 mA, 4 msec) increased the motility index from 2.47 = 0.44 to 11.50 +/- 2.02 (n = 5). This effect was not influenced by the two NO synthase inhibitors N-nitro-L-arginine methyl ester (10(-4) M) and NG-nitro-L-arginine (10(-5) M). However, infusion of inhibitors increased the spontaneous motility index from 2.40 +/- 0.08 to 5.36 +/- 1.08 (P < 0.05) and 3.05 +/- 1.10 to 4.14 +/- 1.04 (P < 0.05), respectively. The addition of L-arginine reversed this effect. Infusion of VIP 2 x 10(-9)M decreased the motility index from 2.32 +/- 0.43 to 1.32 +/- 0.27 (P < 0.05), an effect that was preserved during NO synthase inhibition. Electrical vagus stimulation increased the release of VIP to the venous effluent, an effect that persisted during NO synthase inhibitors. CONCLUSION: We conclude that NO-producing nerves seem to have a tonic inhibitory action on the porcine antral motility, but are not involved in the motor effects of vagal stimulation or VIP infusion.